ALKALI INGESTION DEFINITION Intake through the mouth or nose and subsequent swallowing of a chemical which, in solution, has a pH > 7.0 and is of sufficient strength or quantity to result in injury to tissues. TOXIC CAUSES Any solution with an alkaline pH has the potential to cause tissue injury when ingested. The extent of injury depends not only on pH but also on the volume ingested, contact time, viscosity and concentration. Significant pathology is most commonly observed following ingestions of ammonia, potassium hydroxide, sodium hydroxide or sodium hypochlorite. CLINICAL FEATURES Symptoms and signs associated with significant alkali-induced tissue injury include pain in the mouth and throat, drooling, pain on swallowing, vomiting, abdominal pain and haematemesis. If the larynx is involved, local oedema may produce respiratory distress, stridor and a hoarse voice. Extensive tissue injury may be associated with fever, tachycardia, hypotension and tachypnoea. Inspection of the oropharynx may reveal areas of mucosal burn, which appear as white or grey patches with erythematous borders. The absence of visible burns to the lips, mouth or throat does not necessarily imply an absence of significant burns to the oesophagus. Severe burns from alkali ingestion may lead to the life-threatening complications of oesophageal perforation and mediastinitis. These are associated with chest pain, dyspnoea, fever, subcutaneous emphysema of the chest or neck, and a pleural rub. A chest X-ray may show widening of the mediastinum, pleural effusions, pneumomediastinum and/or pneumothorax. Septic shock, multi-organ failure and death may complicate perforation. Tracheoesophageal fistulae may result from perforation of the anterior oesophageal wall. The fistula may extend to involve the aorta and, in this case, is fatal. An asymptomatic patient is unlikely to have severe injury although asymptomatic children may occasionally have a significant injury. DIFFERENTIAL DIAGNOSIS Acid ingestion Allergic reaction with upper airways involvement Foreign body ingestion Other caustic ingestion Thermal burn Upper airways infection RELEVANT INVESTIGATIONS Upper gastrointestinal endoscopy should be performed as soon as practicable and within 24 hours of ingestion. This investigation is essential to assess the severity of mucosal damage and plan treatment. Upper gastrointestinal endoscopy should also be considered for asymptomatic patients who have intentionally ingested a strong alkali and children, where the history may be unreliable. The following investigations may be useful to evaluate compliations and assist in management: Arterial blood gas analysis Coagulation profile Complete blood count Contrast oesophagography or thoracic CT (to detect oesophageal perforation). ECG Electrolytes Glucose Liver and renal function Radiological studies: Chest x-ray, upright abdominal film Type and cross-match TREATMENT Immediate (first) aid Do not induce vomiting. Do not attempt neutralisation. Do not give oral fluids Do not give oral activated charcoal Do rinse any visible material from the mouth with water or saline Hospital treatment Initial management is primarily supportive. Particular attention should be directed towards securing the airway, fluid resuscitation and provision of opioid analgesia. Do not give activated charcoal as it will interfere with endoscopic evaluation. Ongoing supportive care includes maintenance of adequate analgesia, fluid, electrolyte and pH balance, nutritional support, and monitoring for the development of complications. Subsequent management and prognosis is largely dictated by findings at upper gastrointestinal tract endoscopy. These may be graded as follows: Grade I Simple inflammation. Grade II Few ulcerations, focal necrosis limited to part of the oesophagus. Grade III Multiple ulcerations, extensive necrosis involving all of the oesophagus, massive haemorrhage. Grade I and II lesions should heal completely with supportive care alone and can be adequately managed on a general medical ward. Patients with Grade I lesions will usually tolerate oral fluids but those with Grade II lesions may require a period of total parenteral nutrition or a feeding jejunostomy. Those with grade III endoscopic findings require intensive care management, total parenteral nutrition or a feeding jejunostomy until healing is documented, and are likely to develop oesophageal strictures. Urgent laparotomy (without associated thoracotomy) with surgical resection of necrotic tissue and surgical repair is indicated in the presence of symptoms or signs of gastrointestinal perforation or where full thickness necrosis is found at endoscopy. There is no clinical evidence that corticosteroids prevent the development of strictures following alkali ingestion. Prophylactic broad-spectrum antibiotics are not indicated unless there is evidence of gastrointestinal tract perforation or full thickness necrosis. CLINICAL COURSE AND MONITORING Careful monitoring of respiratory, cardiovascular, and renal systems and fluid, electrolyte and acid-base balance is required. Cases of severe injury should be admitted to an Intensive Care Unit. Close observation is required until an evaluation of the gastrointestinal tract can be made (preferably by endoscopy) unless the patient has become symptom free by that time. Patients should be followed for at least one year following recovery from Grade II or III alkali ingestion. Assessment should be directed toward nutritional status and any problems with swallowing. LONG-TERM COMPLICATIONS Those patients with grade III or circumferential grade II burns are at risk of developing an oesophageal stricture. For this reason, these patients require follow-up evaluations that include endoscopic examination and/or contrast radiography until complete healing or stricture formation is documented. Eighty percent of strictures produce symptoms within two months. Oesophageal stricture formation requires long-term dilation or surgical repair. Survivors of alkali ingestion are at an increased risk of developing carcinoma of the oesophagus. The average interval between the original injury and diagnosis of carcinoma is greater than 40 years. AUTHOR(S)/REVIEWERS Author: Robert Dowsett Consultant Toxicologist Departments of Clinical Pharmacology and Emergency Medicine Westmead Hospital Westmead, NSW 2145 Australia Peer Review: Geneva 8/98: D. Jacobsen, L. Murray, J. Pronczuk. Birmingham 3/99: T. Meredith, L. Murray, A. Nantel, J. Szajewski.